Repeated electroconvulsive shock (ECS) was administered to rats previously injected with DSP-4 (N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride), a noradrenergic neurotoxin. The normal increase in neocortical beta 1-adrenoceptor binding caused by noradrenaline depletion was effectively prevented by ECS. This finding suggests that the plasticity of the beta 1-adrenoceptor may be partially independent of endogenous noradrenaline concentration. Additionally, functional noradrenergic neurons are not necessarily a critical requirement for the antidepressant effect of electroconvulsive treatment in humans.